1. Field of the Invention
The invention relates to a heart monitoring apparatus. According to a preferred aspect of the invention, the heart monitoring apparatus is incorporated in an implantable medical device such as an implantable pacemaker, implantable cardioverter/defibrillator or a combination thereof.
2. Description of the Related Art
Such implantable medical devices are used to help patients suffering from some type of heart failure (HF) such as congestive heart failure (CHF) and the like. The implantable medical device shall ideally choose a therapy mode best suiting a patient's health state by automatic determination of the health state.
A typical pacemaker has at least one stimulation pulse generator to selectively generate stimulation pulses for delivery to at least two different chambers of a heart, said chambers include right and left atria and right and left ventricles. Said one stimulation pulse generator may be switchable in order to generate stimulation pulses for different chambers of the heart. In general, however, separate stimulation pulse generators will be provided for each heart chamber to be stimulated. The timing and triggering of stimulation pulses is typically controlled by a control unit. Time intervals to be timed by the control unit may, among other things, include an atrioventricular time delay (AVD) between an atrial event and a ventricular event and/or an interventricular delay (VVD) between a right ventricular event and a left ventricular event.
State of the art pacemakers include means to optimize the atrioventricular and/or the interventricular delay based on a hemodynamic sensor information.
For AVD optimization, the pacemaker provides for at least one atrial and one ventricular channel for pacing and/or sensing. For VVD optimization, the pacemaker provides for pacing channels for both ventricles.
A pacemaker shall help a heart suffering from some disorder to perform similarly to a healthy heart.
In a healthy heart, initiation of the cardiac cycle normally begins with depolarization of the sinoatrial (SA) node. This specialized structure is located in the upper portion of the right atrium wall and acts as the natural “pacemaker” of the heart. In a normal cardiac cycle and in response to the initiating SA depolarization, the right atrium and left atrium contract and force the blood that has accumulated therein into the ventricles. The natural stimulus causing the right atrium and left atrium to contract is conducted to the right ventricle and left ventricle via the atrioventricular node (AV node) with a short, natural delay, the atrioventricular delay (AV-delay, AVD). Thus, a short time after the right atrial and left atrial contraction (a time sufficient to allow the bulk of the blood in the atria to flow through the one-way valves into the ventricles), the ventricles contract, forcing the blood out of the ventricles to the lungs and body tissue. A typical time interval between contraction of the atria and contraction of the ventricles might be 60 ms; a typical time interval between contraction of the ventricles and the next contraction of the atria might be 800 ms. Thus, it is a right atrial and left atrial contraction (A), followed a relatively short time thereafter by a right ventricle and left ventricle contraction (V), followed by a relatively long time thereafter by the next right atrial and left atrial contraction, that produces the desired AV synchrony. Where AV synchrony exists, the heart functions very efficiently as a pump in delivering life-sustaining blood to body tissue; where AV synchrony is absent, the heart functions as an inefficient pump (largely because the right ventricle is contracting when it is not maximally filled with blood).
In addition to proper filling time with respect to the atria, the positive or negative time delay between the right and left ventricles determines the degree to which they provide a mechanical advantage to each other during contraction due to their common point of attachment (the apex) and shared wall (the septum).
A pacemaker generally shall induce a contraction of a heart chamber by delivery of a stimulation pulse (pacing pulse) to said chamber when no natural (intrinsic) stimulation of said chamber occurs in due time. A contraction of a heart chamber often is called “event.” Since a stimulation may be an intrinsic stimulation, which can be sensed by a sensing stage of a pacemaker, such event is called a sensed event. A stimulation due to delivery of a stimulation pulse is called a paced event. A sensed event in the atrium is called As, a paced atrial event is called Ap. Similarly, a sensed event in the ventricle is called Vs and a paced ventricular event is called Vp.
To mimic the natural behavior of a heart, a dual-chamber pacemaker provides for an AV-delay timer to provide for an adequate time delay (AV-delay, AVD) between a natural (intrinsic) or a stimulated (paced) right atrial stimulation and a right ventricular stimulation. In a similar way, a biventricular pacemaker provides for an adequate time delay (VV-delay, VVD) between a right ventricular stimulation and a left ventricular stimulation.
The time delay for a left ventricular (stimulated, paced) contraction may be timed from a scheduled right ventricular stimulation, which has not yet occurred or from a natural (intrinsic) or a stimulated (paced) right atrial contraction. In the latter case, a left ventricular stimulation pulse is scheduled by a time interval AVD+VVD.
To deal with possibly occurring natural (intrinsic) atrial or ventricular stimulations, a demand pacemaker schedules a stimulation pulse for delivery at the end of the AV-delay or the VV-delay, respectively. The delivery of said stimulation pulse is inhibited, if a natural stimulation of the heart chamber to be stimulated is sensed within the respective time delay.
Ventricular pacing in one or both ventricles is required for patients with AV-block and for CHF patients that are indicated for cardiac resynchronization therapy (CRT). For patients with intact sinus rhythm or with effective atrial pacing, it is beneficial to stimulate the ventricle(s) synchronous with the atrial activation, i.e., after a certain delay period after the atrial event. Standard AV-synchronous dual- or three-chamber implantable devices have a programmable AVD that can be adjusted by the physician. Several studies have shown the importance of individual AVD optimization to improve the cardiac output. Especially for CHF patients, optimization of the AVD is essential. As the pumping efficacy is impaired, the optimal timing of the ventricular stimulus in relation to the atrial event contributes significantly to the cardiac performance. If the AVD is too short, the ventricle contracts before it is completely filled by the atrial blood inflow. The active filling time is reduced. Hence the stroke volume and the cardiac output are reduced. If the AVD is too long, the ventricle contracts a while after the closure of the atrioventricular valve. Hence the passive filling time of the ventricle, i.e., the diastolic filling period during the myocardial relaxation before the atrial kick, is decreased. Also backflow of blood from the ventricle into the atrium, e.g., mitral regurgitation, is likely. Thus also in this case cardiac output (CO) is reduced. Similar to the heart rate, the optimal AVD also depends on the activation state of the circulation. If the sympathetic tone is high, e.g., during exercise, the optimal AVD is shortened compared to the resting value.
Patients with CHF and Left Bundle-Branch Block (LBBB), i.e., with interventricular dyssynchrony expressed by a widened QRS complex in the electrogram, may benefit from biventricular pacing. Pacing both ventricles simultaneously or with a certain VVD restores the synchrony of the ventricles and thus improves the hemodynamic performance. Also mitral regurgitation may be reduced by biventricular pacing. Recent CRT pacing devices, implantable pulse generators (IPGs) or ICDs, offer a programmable VVD parameter. The delay time between the right ventricular (RV) and left ventricular (LV) stimulation can be programmed, usually approx. in the range −100 ms . . . +100 ms. The sign determines whether the RV or the LV is paced first. 0 ms means simultaneous pacing of both ventricles. Also RV or LV-only pacing can be programmed. It has been found that the setting resulting in optimal hemodynamics varies individually from patient to patient. The optimal value also depends on the individual position of the left ventricular pacing lead, which usually is located in a lateral coronary vein, or less often on the left epicardium.
Some prior art pacemakers include at least one impedance measuring stage being connected to electrodes or a connector for such electrodes to measure an intracardiac impedance when in use.
For CRT optimization presently the following techniques are applied:    1. Echocardiographic techniques to optimize AV and/or VV intervals that are expensive, time consuming and can only be done periodically, not continuously. These techniques are frequently unreliable and poorly reproducible.    2. Automatic AV/VV optimization at Follow up based on intracardiac electric assumptions. This is not a continuous method, and while less costly and less time consuming than echo, it is still periodic. Clinical utility and reproducibility of these methods remain to be proven.
To monitor heart failure status presently the following techniques are applied:    1. Monitoring of pulmonary edema. Pulmonary edema is a very late sign of worsening heart failure. So far, the sensitivity and specificity of the known monitor have been low (approx 60%).    2. Direct monitoring of left atrial pressure. This requires a separate sensor (from IMD and leads) and directly accesses the left atrium which could put a patient at increased risk of bleeding, infection, or embolism.
Problems Not Solved so Far are:
Early detection of HF before the development of pulmonary edema. Reveal this early stage by monitoring transthoracic and intracardiac impedance signals.
Atypical forms of HF may not show usual signs, for example, HF may show no indication of conduction system defect or change in QRS width. The proposed solution is to reveal this atypical HF by detecting the weakening of the relationship between the electrical and mechanical events of LV function caused by a developing HF.
30% of patients with CRT are non-responders. The proposed solution is to optimize CRT by tracking the response to therapy by monitoring electromechanical coupling events and adjusting IMD parameters automatically.
Objective measures of optimal medical therapy for the treatment of HF do not exist. The proposed solution identifies a device-based measure that can determine a physiological (i.e. electromechanical coupling) response to medical intervention.